Abstract: Stroke is one of the leading causes of death and disability, especially for the old population in modern world.As one of ligand-gating ionotropic glutamate receptors, N-methyl-D-aspartate rece pto r(NMDAR)involves in excitatory synaptic transmission, synaptic plasticity and the cause and development of numerous neurological as well as psychiatric disorders.Since the distribution of NMDAR varies in different regions, certain brain regions such as hippocampus and cortex with the highest density of NMDAR, are especially sensitive to ischemia.Much emphasizes have been put on the changes of excitatory neurotransmission and NMDAR in central nervous system after ischemia, because the glutamate-mediated excitatory neurotoxicity play a key role in the development of stroke.It has been shown that neuronal death after ischemia results from excessive Ca²⁺ influx, which is due to the hyperactivity of NMDAR, Ca²⁺ permeable α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor, kainic acid receptors and/or other ion channels permeable to Ca²⁺.The increase of intracellular Ca²⁺ triggers the cascades of cell death.With specific structure and pharmacology properties, this study of the tracer of NMDAR give the target for early diagnosis and developing of specific antagonist.Elucidating the changes in interneurons after ischemia/ hypoxia with tomography in vivo will help to understand the mechanisms underlying the neoroprotection of antagonist.